Raptor (regulatory-associated protein of TOR) is the defining scaffold subunit of TOR complex 1 (TORC1), composed of an N-terminal caspase-like domain, HEAT repeats and a C-terminal WD40 beta-propeller. Raptor binds TOR and recruits TORC1 substrates such as S6K and 4E-BP/Thor, and in other species couples TORC1 to amino-acid signals through binding to Rag GTPases. In Drosophila, raptor is required for TORC1-dependent S6K Thr398 phosphorylation, cell growth and cell size, for suppression of autophagy (including in the developmentally dying larval midgut), for TORC1-mediated negative feedback on insulin/Akt signaling, and in muscle for normal development and eclosion.
| GO Term | Evidence | Action | Reason |
|---|---|---|---|
| GO:0005737 cytoplasm | IBA GO_REF:0000033 | ACCEPT | Summary: Cytoplasm (phylogenetic inference). Reason: TORC1 acts in the cytoplasm; no more specific fly location is established in cached evidence. |
| GO:0007517 muscle organ development | IMP PMID:25866192 The role of TORC1 in muscle development in Drosophila. | KEEP AS NON CORE | Summary: Muscle-specific raptor knockdown prevents eclosion. Reason: Tissue-specific developmental consequence of TORC1 loss. Supporting Evidence: PMID:25866192 muscle-specific knockdown of Raptor causes flies to be too weak to emerge from their pupal cases during eclosion |
| GO:0007562 eclosion | IMP PMID:25866192 The role of TORC1 in muscle development in Drosophila. | KEEP AS NON CORE | Summary: Muscle-specific raptor knockdown prevents eclosion. Reason: Tissue-specific developmental consequence of TORC1 loss. Supporting Evidence: PMID:25866192 muscle-specific knockdown of Raptor causes flies to be too weak to emerge from their pupal cases during eclosion |
| GO:0008286 insulin receptor signaling pathway | IMP PMID:17183368 Insulin delays the progression of Drosophila cells through G... | KEEP AS NON CORE | Summary: Insulin effects on G2/M are mediated by dTOR/dRaptor. Reason: Pathway context (same decision as mTor). Supporting Evidence: PMID:17183368 Insulin's effects on progression through G2/M are mediated by dTOR/dRaptor signalling. |
| GO:0008286 insulin receptor signaling pathway | IMP PMID:20585550 Dynamic switch of negative feedback regulation in Drosophila... | KEEP AS NON CORE | Summary: Raptor knockdown enhances Akt phosphorylation (TORC1 negative feedback). Reason: Raptor/TORC1 acts in the insulin pathway, both downstream and as a source of negative feedback on Akt; pathway-context annotation. Supporting Evidence: PMID:20585550 Under wild-type conditions, negative feedback to the PI3K/Akt signaling branch is mediated by TORC1 (containing TOR, Lst8 and Raptor), independently of S6K. |
| GO:0008340 determination of adult lifespan | IMP PMID:25866192 The role of TORC1 in muscle development in Drosophila. | KEEP AS NON CORE | Summary: Lifespan of muscle raptor knockdown flies. Reason: Organism-level consequence; the paper notes that surviving knockdown flies generally had normal lifespan, so the role is modest. Supporting Evidence: PMID:25866192 The lifespan of these Raptor knockdown flies was measured to determine the effects of dTORC1 suppression on longevity. |
| GO:0009267 cellular response to starvation | IBA GO_REF:0000033 | KEEP AS NON CORE | Summary: Cellular response to starvation (phylogenetic inference, yeast donor). Reason: TORC1 inactivation is part of the starvation response; inherited, non-core. |
| GO:0010506 regulation of autophagy | IBA GO_REF:0000033 | MODIFY | Summary: Regulation of autophagy (phylogenetic inference). Reason: The direction is known: raptor depletion causes premature autophagy, so TORC1 negatively regulates (macro)autophagy; replaced with the specific term used for mTor. Propagation Review Root cause: TERM SCOPING PROBLEM Sources checked: PANTHER:PTN000304084 SUPPORTS TRANSFER Transfer is sound; the inherited term is more general than the target's own experimental evidence supports. Proposed replacements: negative regulation of macroautophagy Supporting Evidence: PMID:25882046 raptor depletion resulted in premature autophagy similar to Tor ablation, suggesting that raptor and Tor function in TORC1 and negatively regulates autophagy in this cell death context |
| GO:0030307 positive regulation of cell growth | IBA GO_REF:0000033 | ACCEPT | Summary: Positive regulation of cell growth (phylogenetic inference). Reason: Consistent with fly raptor knockdown data on S6K-induced overgrowth and cell size. Supporting Evidence: PMID:17462592 However, the knockdown of another TOR binding partner, raptor, decreased S6K-Thr-398 phosphorylation and inhibited S6K-induced cell overgrowth. |
| GO:0030674 protein-macromolecule adaptor activity | IBA GO_REF:0000033 | ACCEPT | Summary: Raptor acts as a protein-macromolecule adaptor (phylogenetic inference). Reason: Raptor is a scaffold that brings TORC1 substrates (S6K, 4E-BP) to the TOR kinase; the IBA (donor human RPTOR, PTN000304084) is consistent with fly data that raptor is needed for S6K phosphorylation. Supporting Evidence: PMID:17462592 However, the knockdown of another TOR binding partner, raptor, decreased S6K-Thr-398 phosphorylation and inhibited S6K-induced cell overgrowth. |
| GO:0031929 TOR signaling | IEA GO_REF:0000002 | MODIFY | Summary: TOR signaling (InterPro). Reason: Correct but general; Raptor is TORC1-specific and already carries TORC1 signaling. Proposed replacements: TORC1 signaling Supporting Evidence: PMID:25882046 TOR can assemble into distinct complexes, TORC1 and TOCR2, with Raptor and Rictor, respectively. |
| GO:0031931 TORC1 complex | IBA GO_REF:0000033 | ACCEPT | Summary: Raptor is the defining subunit of TORC1. Reason: Core complex membership. Supporting Evidence: PMID:22493059 In mutants lacking LST8, expression of TOR and RAPTOR, together with their upstream activator Rheb, was sufficient to provide TORC1 activity and stimulate cell and organ growth. |
| GO:0031931 TORC1 complex | IDA PMID:22493059 LST8 regulates cell growth via target-of-rapamycin complex 2... | ACCEPT | Summary: Raptor is the defining subunit of TORC1. Reason: Core complex membership. Supporting Evidence: PMID:22493059 In mutants lacking LST8, expression of TOR and RAPTOR, together with their upstream activator Rheb, was sufficient to provide TORC1 activity and stimulate cell and organ growth. |
| GO:0031931 TORC1 complex | IEA GO_REF:0000002 | ACCEPT | Summary: Raptor is the defining subunit of TORC1. Reason: Core complex membership. Supporting Evidence: PMID:22493059 In mutants lacking LST8, expression of TOR and RAPTOR, together with their upstream activator Rheb, was sufficient to provide TORC1 activity and stimulate cell and organ growth. |
| GO:0035096 larval midgut cell programmed cell death | IMP PMID:25882046 Distinct requirements of Autophagy-related genes in programm... | KEEP AS NON CORE | Summary: Raptor knockdown accelerates autophagy and midgut cell death. Reason: Context-specific consequence of TORC1 regulation of autophagy (same decision as mTor). Supporting Evidence: PMID:25882046 Consistent with this role of TORC1, knockdown of raptor resulted in earlier autophagy induction and smaller midguts, whereas rictor knockdown had no effect |
| GO:0038202 TORC1 signaling | IBA GO_REF:0000033 | ACCEPT | Summary: Raptor mediates TORC1 signaling. Reason: Core process. Supporting Evidence: PMID:17462592 However, the knockdown of another TOR binding partner, raptor, decreased S6K-Thr-398 phosphorylation and inhibited S6K-induced cell overgrowth. |
| GO:0038202 TORC1 signaling | IMP PMID:22493059 LST8 regulates cell growth via target-of-rapamycin complex 2... | ACCEPT | Summary: Raptor mediates TORC1 signaling. Reason: Core process. Supporting Evidence: PMID:17462592 However, the knockdown of another TOR binding partner, raptor, decreased S6K-Thr-398 phosphorylation and inhibited S6K-induced cell overgrowth. |
| GO:0038202 TORC1 signaling | NAS PMID:22493059 LST8 regulates cell growth via target-of-rapamycin complex 2... | ACCEPT | Summary: Raptor mediates TORC1 signaling. Reason: Core process. Supporting Evidence: PMID:17462592 However, the knockdown of another TOR binding partner, raptor, decreased S6K-Thr-398 phosphorylation and inhibited S6K-induced cell overgrowth. |
| GO:0045793 positive regulation of cell size | IMP PMID:19216764 PDGF/VEGF signaling controls cell size in Drosophila. | ACCEPT | Summary: Raptor silencing reduces S2R+ cell size. Reason: Principal TORC1 output, same decision as for mTor. Supporting Evidence: PMID:19216764 Silencing positive regulators of the pathway (Rheb, Tor, Raptor and S6k) led to a significant decrease in cell size |
| GO:0045886 negative regulation of synaptic assembly at neuromuscular junction | IMP PMID:23393158 Tuberous sclerosis complex regulates Drosophila neuromuscula... | UNDECIDED | Summary: Raptor and NMJ synaptic growth. Reason: The cached abstract (no full text) reports that raptor knockdown did not phenocopy the increased synaptic growth of Tsc2 and rictor mutants, which does not support a negative regulatory role for raptor; the curator's full-text basis cannot be verified. Supporting Evidence: PMID:23393158 Increased synaptic growth was also observed in rictor mutants, while raptor knockdown did not phenocopy the TSC mutant phenotype |
| GO:0048477 oogenesis | IMP PMID:24786828 The TORC1 inhibitors Nprl2 and Nprl3 mediate an adaptive res... | KEEP AS NON CORE | Summary: Raptor/TORC1 in oogenesis under amino-acid limitation. Reason: Developmental context of TORC1 signaling in the germline; the cached abstract (no full text) does not mention raptor, so the row is kept, deferring to the curator. |
| GO:0071230 cellular response to amino acid stimulus | IBA GO_REF:0000033 | KEEP AS NON CORE | Summary: Cellular response to amino acid stimulus (phylogenetic inference). Reason: Raptor couples TORC1 to amino-acid signals (via Rag binding in other species; IBA donor human RPTOR); no fly-specific raptor evidence is cached. Kept as non-core. |
| GO:1902669 positive regulation of axon guidance | IGI PMID:22319582 Diet and energy-sensing inputs affect TorC1-mediated axon mi... | UNDECIDED | Summary: Raptor knockdown rescues Rheb-induced axon misrouting. Reason: Raptor knockdown suppresses gain-of-function axon misrouting caused by Rheb overexpression; this shows TORC1 hyperactivity disrupts guidance, so a positive regulation of axon guidance is not clearly supported (same decision as for mTor). Supporting Evidence: PMID:22319582 Knockdown of raptor resulted in almost complete rescue of Rheb-mediated axon guidance defects |
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Download this section (compressed HTML)raptor (raptor) encodes a crucial component of target of rapamycin (TOR) complex 1, which is a conserved regulator of cell growth and metabolism.
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